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Early Postnatal Lipopolysaccharide Exposure Leads to Enhanced Neurogenesis and Impaired Communicative Functions in
Yi Pang1, Xuemei Dai1, Anna Roller2
1Department of Pediatrics, University of Mississippi Medical Center, Jackson, Mississippi, United States of America.
Plos One
|October 11, 2016
Summary
Early-life inflammation from lipopolysaccharide (LPS) alters microglia phenotypes, impacting neural development and causing cognitive deficits. M2-like microglia activation may contribute to autism spectrum disorder (ASD)-like behaviors.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Perinatal infections are linked to neurodevelopmental disorders like white matter injury (WMI) and autism spectrum disorders (ASD).
- Mechanisms connecting early inflammation to aberrant neural development are not fully understood.
Purpose of the Study:
- To investigate the effects of lipopolysaccharide (LPS)-induced neuroinflammation on microglia phenotypes and early neural development in rats.
- To explore the relationship between microglial activation, neural development, and behavioral outcomes.
Main Methods:
- Rats were exposed to LPS on postnatal day 3 to induce systemic neuroinflammation.
- Microglia phenotypes (M1/M2), apoptosis, cell proliferation, and oligodendrocyte lineage populations were assessed.
- Communicative and cognitive functions were evaluated in LPS-exposed rats.
Main Results:
- LPS exposure induced mixed M1 and M2 microglial activation, with M2 markers strongly upregulated in specific brain regions.
- A decrease in apoptosis and an increase in cell proliferation were observed in the subventricular zone and dentate gyrus.
- LPS-exposed rats showed increased oligodendrocyte lineage cells and significant impairments in communicative and cognitive functions.
Conclusions:
- M2-like microglial activation may play a role in abnormal neural development following early-life inflammation.
- These neurodevelopmental alterations could underlie autism spectrum disorder (ASD)-like behavioral impairments.
